neurodevelopmental etiology Flashcards

1
Q

in 1980, crow developed:

A

type 1 and type 2 schizophrenia

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2
Q

focus of type 1 and type 2 schizophrenia:

A

primarily structural changes after the onset

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3
Q

some brain imaging machines:

A

CAT or CT scan, PET scan, MRI, fMRI, DTI

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4
Q

the development of what created PET scan?

A

radioligands

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5
Q

CT scan uses:

A

X-rays of the head taken from many directions then processed using computer program

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6
Q

MRI uses:

A

strong magnetic fields, magnetic field gradients, and radio waves to generate complete images of brain

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7
Q

PET scan uses:

A

radioactive substances known as radio tracers to visualize and measure changes in metabolic processes and in physiological activities

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8
Q

fMRI uses:

A

MRI techniques by detecting changes associated with blood flow

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9
Q

Diffusion tenor imagine (DTI) uses:

A

MRI technique that measures diffusion of water in tissue in order to produce neural tract images

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10
Q

early CT studies detect larger:

A

lateral ventricles possibly suggesting loss of brain matter

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11
Q

early MRI studies detect reductions in:

A

overall brain size

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12
Q

Later MRI studies demonstrate reductions in/gets worse with:

A

thickness of the cortex that is present at the onset of illness and gets worse with disease progression

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13
Q

neurodevelopmental hypothesis:

A

not only is schizophrenia associated with structural pathology, data has also suggested that the pathology is in the form of a structural defect

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14
Q

the brain takes years of fine tuning before the brain functions in the:

A

same way as an adult and has adult like microstructure

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15
Q

synaptogensis:

A

neurons start making connections and sends out projections to nearby neurons. synapse formation begins contributing in part of growth of grey matter

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16
Q

grey matter changes in childhood to adolescence:

A

cortical thickness decreases, synapses rearranged and pruned, greater efficiency

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17
Q

white matter changes in childhood to adolescence:

A

myelination increases, greater connectivity, greater efficiency

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18
Q

synapse rearrangement steps: (3)

A
  1. release and uptake of neurotrophic factors
  2. neurons receiving insufficient neurotropic factors die
  3. axonal processes complete for limited neurotropic factor
19
Q

active synapses likely take up:

A

neurotrophic factors that maintains the synapse

20
Q

inactive synapses get too little:

A

trophic factors to maintain stable

21
Q

more synapses equals ____ cortex

22
Q

pruned synapses equals ____ cortex

23
Q

possibility 1 of schizophrenia as a neurdevelopmental disorder:

A

presence of an early developmental “insult” that is latent throughout development but not does manifest behaviorally until later when brain can no longer compensate

24
Q

possibility 2 of schizophrenia as a neurdevelopmental disorder:

A

imbalance in inhibitory and excitatory neural activity isn’t a big deal until adolescence is required for the “fine tuning” of higher cognitive function

25
table stages of schizophrenia diagnostics:
features, diagnosis, disability, intervention
26
evidence for disruptions in brain development have been identified at every:
stage of schizophrenia
27
primary differences in brain of those with schizo and healthy brain (3)
1. deficits in myelination (reduced communication) 2. earlier decline in prefrontal excitatory synapses ( excessive pruning) 3. deficit in the development of inhibitory synapses (reduced interneuron activity)
28
primary cell types include those that are involved in:
dopamine and glutamate signaling
29
glutamate responsible for:
learning and memory
30
dopamine located in ___ parts of brain and glutamate located in ___ part of brain:
midbrain and striatum; cortex
31
mesocortical pathway responsible for:
cognitive and executive function
32
negative symptoms are:
HYPOdopaminergic
33
mesolimbic pathway responsible for:
regulation of emotional behavior
34
positive symptoms are:
HYPERdopaminergic
35
tuberinfundibular pathway responsible for:
regulation of prolactin secretion
36
nigrostriatal pathway responsible for:
motor control
37
in the shchizo brain, dopamine levels in the mesolimbic pathway are:
increase causing positive symptoms of schizo. high levels
38
dopamine levels in the mesocortical pathway are:
decreased, leading to negative and cognitive symptoms. low levels
39
the predominant "go" neurotransmitter in the brain is:
glutamate
40
evidence implicating glutamate hypothesis: (3)
1. post mortem changes in NMDA receptors 2. NMDA-recoptor antagonists can cause psychotic symptoms 3. some glutamatergic drugs have shown promise in treated schizo
41
steps in glutamatrgic and dopaminergic pathways: (4)
1. reduced NMDA receptor availability/ functioning on GABAergic interneurons 2. disinhibition of glutamatrgic projections onto midbrain dopamine neurones 3. increase glutamate release 4. increase activation of dopaminergic neurones
42
most glutamtergic excitatory synapses occur one small protrusions along dendrites called:
dendritic spines
43
during development and adulthood, changes in dendritic spine number and shape accompany:
synapse formation, cell maintenance, and cell elimination allowing remodeling of connectivity within neuronal circuits
44